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PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Normal Chow diet]

ABSTRACT: PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Normal Chow diet]

PROVIDER: PRJNA1102893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28759752.fastq.gz	Fastqsanger.gz
	SRR28759753.fastq.gz	Fastqsanger.gz
	SRR28759754.fastq.gz	Fastqsanger.gz
	SRR28759755.fastq.gz	Fastqsanger.gz
	SRR28759756.fastq.gz	Fastqsanger.gz

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PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Normal Chow diet]

Project description:Somatic mutations in non-malignant tissues are selected for because they confer increased clonal fitness, however, it is uncertain if these clones can benefit organ health. Here, ultra-deep targeted sequencing of 150 liver samples from 30 chronic liver disease patients revealed recurrent somatic mutations. PKD1 mutations were observed in 30% of patients, whereas they were only detected in 1.3% of hepatocellular carcinomas (HCCs). To interrogate tumor suppressor functionality, we perturbed PKD1 in two HCC cell lines and six in vivo models, in some cases showing that PKD1 loss protected against HCC, but in most cases showing no impact. However, Pkd1 haploinsufficiency accelerated regeneration after partial hepatectomy. We tested Pkd1 in fatty liver disease, showing that Pkd1 loss was protective against steatosis and glucose intolerance. Mechanistically, Pkd1 loss selectively increased mTOR signaling without SREBP activation. In summary, PKD1 mutations in cirrhotic livers exert adaptive functionality without increasing transformation risk.

2024-05-15 | GSE264520 | GEO

PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Western Diet + CCl4]

2024-05-15 | GSE264521 | GEO

PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Western Diet + CCl4]

Project description:PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Western Diet + CCl4]

| PRJNA1102894 | ENA

Gene expression profiling unravels cancer-related hepatic molecular signatures in steatohepatitis but not in steatosis

Project description:Pathogenesis and factors for determining progression of alcoholic and non-alcoholic steatosis to steatohepatitis with risk of further progression to liver cirrhosis and cancer are poorly understood. In the present study, we aimed to identify potential molecular signatures for discrimination of steatohepatitis from steatosis. Global gene expression analysis was applied to unravel differentially expressed genes between steatohepatitis compared to steatosis and control samples. For functional annotation as well as the identification of disease-relevant biological processes of the differentially expressed genes the gene ontology (GO) database was used. Genes down-regulated in steatohepatitis were mainly involved in metabolic processes. Genes up-regulated in steatohepatitis samples were associated with cancer progression and proliferation. Further statistical and pathway analysis lead to the selection of 46 candidate genes which were validated in two sample cohorts by quantitative real-time PCR. In surgical liver resection samples 39 genes and in percutaneous liver biopsies 30 genes were significantly up-regulated in steatohepatitis. Conclusion: The development of steatohepatitis is characterized by distinct molecular changes. 44 human liver tissue surgical samples (normal n=13; steatosis n=19; steatohepatitis n=12, 8/2 cirrhotic/non-cirrhotic) obtained from patients undergoing liver surgery for HCC, other malignancy/metastatic disease, benign tumors of the liver and organ dedicated to transplantation. Virtually normal control samples in this cohort were taken from patients undergoing surgical resection of liver metastasis, but the surrounding liver tissue used for the molecular analyses was normal, non-tumorous liver tissue without detectable pathological changes. The samples were provided by the Biobank at the Medical University of Graz. This dataset is part of the TransQST collection.

2012-12-10 | E-GEOD-33814 | biostudies-arrayexpress

PKD1

Project description:PKD1 gene and protein study

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Project description:PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer

| PRJNA1102869 | ENA

Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression [Pkd1]

Project description:We report the findings of deletion of the miR17 binding motif from Pkd1 mRNA

2022-02-11 | GSE196588 | GEO

Dehydration facilitates cyst formation and growth in Pkd1-/- mice via macrophage

Project description:The Pkd1 gene was inactivated by tamoxifen at postnatal day 30 (P30) to generate a chronic-onset conditional Pkd1 gene knockout mouse model. Without any intervention, micro cysts could be detected adjacent to renal medulla-corticomedullary junction in Pkd1-/- mice until P180 and cystic phenotype is severe at P300. However, under dehydration situation, the cyst growth was more accelerated and progressive. The dehydration protocol resulted in Pkd1-/- mice varying degrees of sweating and weight loss. Mice that were not provided water during the day (water at night (D-WAN)) and mice that had access to water during the day (water all time (D-WAT)) showed significantly more weight loss compared with the control Pkd1-/- mice, although they drank more water at night. Interestingly, although D-WAN Pkd1-/- mice and D-WAT Pkd1-/- mice lost approximately body weights after one-day dehydration, while cyst enlargement and renal dysfunction was much more severe in the D-WAN Pkd1-/- mice after two-month intervention.

2021-04-27 | E-MTAB-10449 | biostudies-arrayexpress

Identification of the proteins secreted by normal and cirrhotic LSECs

Project description:Normal and cirrhotic LSECs can influence hepatic stellate cells (HSCs) differently. This project aims to determine the set of proteins secreted by LSECs from healthy and cirrhotic livers, and identify the protein(s) that promote HSC activation.

2018-11-06 | PXD009010 | Pride

Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression [Pkd1]

Project description:Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression [Pkd1]

| PRJNA805542 | ENA